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Biomedical subjects

E H Burger

Publications and source records attributed to E H Burger.

At least 19 recordsLinked to original sources
PubMed2002

Bone histomorphometric evaluation of a clinically fused titanium tumour cage in a child.

An intervertebral titanium tumour cage was implanted in a 2-year-old-girl after T11 spondylectomy due to Ewing sarcoma. After 2-years' follow-up without evidence of recurrence, the titanium cage was explanted to correct spinal deformity and to allow normal spinal growth development. Radiological follow-up and surgical exploration at the time of retrieval suggested fusion of the segment. Histologic evaluation, however, demonstrated ingrowth of trabecular bone, but without bridging trabecular bone. The distance between the opposing bone fronts measured 1.5 mm and the viable bone volume (BV/TV) within the cage was 36%. Histologic evaluation demonstrated that bone formation was still an ongoing process in the fusion zone 2 years after implantation.

Child, Preschool↗
PubMed2002

In vitro and in vivo degradation of bioabsorbable PLLA spinal fusion cages.

The in vitro and in vivo degradation of poly-L-lactic acid cages used as an adjunct to spinal arthrodesis was investigated. In the in vitro experiments cages were subjected to aging up to 73 weeks in phosphate-buffered solution (pH 7.4) at 37 degrees C. Inherent viscosity, crystallinity, and mechanical strength were determined at different time points. In the in vivo study, the poly-L-lactic acid cages were packed with bone graft and implanted in the L3-L4 spinal motion segment of 18 Dutch milk goats. At 12, 26, and 52 weeks, the motion segments were isolated and poly-L-lactic acid samples retrieved. On evaluation, the in vivo implanted cages showed an advanced decline in inherent viscosity compared to the cages subjected to in vitro degradation experiments. At 6 months of implantation, the geometrical shape and original height of 10 mm was maintained during 6 months of follow up. This finding fits well with the observation that mechanical strength was maintained for a period of 6 months in vitro. At 12 months, the poly-L-lactic acid cage had been disintegrated into multiple fragments with signs of absorption. Despite the high-load-bearing conditions, the poly-L-lactic acid cage allowed interbody fusion to occur without collapse of the cage.

Absorption↗
PubMed2002

Transforming growth factor-beta1 incorporation in a calcium phosphate bone cement: material properties and release characteristics.

The bone regenerative properties of calcium phosphate cements (CPCs) may be improved by the addition of growth factors, such as recombinant human transforming growth factor-beta1 (rhTGF-beta1). Previously, we showed that rhTGF-beta1 in CPC stimulated the differentiation of preosteoblastic cells from adult rat long bones. The intermixing of rhTGF-beta1 in CPC, which was subsequently applied to rat calvarial defects, enhanced bone growth around the cement and increased the degradation of the cement. However, it is unknown whether the addition of rhTGF-beta1 changes the material properties of CPC and what the characteristics of the release of rhTGF-beta1 from CPC are. Therefore, we determined in this study the release of rhTGF-beta1, in vitro, from the cement pellets as implanted in the rat calvariae. The possible intervening effects of rhTGF-beta1 intermixing on the clinical compliance of CPC were studied through an assessment of its compressive strength and setting time, as well as its crystallinity, calcium-to-phosphorus ratio, porosity, and microscopic structure. We prepared CPC by mixing calcium phosphate powder (58% alpha-tricalcium phosphate, 25% anhydrous dicalcium phosphate, 8.5% calcium carbonate, and 8.5% hydroxyapatite) with a liquid (3 g/mL). The liquid for standard CPC consisted of water with 4% disodium hydrogen phosphate, whereas the liquid for modified CPC was mixed with an equal amount of 4 mM hydrochloride with 0.2% bovine serum albumin. The hydrochloride liquid contained rhTGF-beta1 in different concentrations for the release experiments. Most of the rhTGF-beta1 incorporated in the cement pellets was released within the first 48 h. For all concentrations of intermixed rhTGF-beta1 (100 ng to 2.5 mg/g of CPC), approximately 0.5% was released in the first 4 h, increasing to 1.0% after 48 h. Further release was only about 0.1% from 2 days to 8 weeks. CPC modification slightly increased the initial setting time at 20 degrees C from 2.6 to 5 min but had no effect on the final setting time of CPC at 20 degrees C or the initial and final setting times at 37 degrees C. The compressive strength was increased from 18 MPa in the standard CPC to 28 MPa in the modified CPC only 4 h after mixing. The compressive strength diminished in the modified CPC between 24 h and 8 weeks from 55 to 25 MPa. No other significant change was found with the CPC modification for rhTGF-beta1. X-ray diffraction revealed that standard and modified CPCs changed similarly from the original components, alpha-tricalcium phosphate and anhydrous dicalcium phosphate, into an apatite cement. The calcium-to-phosphorus ratio, as determined with an electron microprobe, did not differ for standard CPC and modified CPC. Standard and modified CPCs became dense and homogeneous structures after 24 h, but the modified CPC contained more crystal plaques than the standard CPC, as observed with scanning electron microscopy (SEM). SEM and back- scattered electron images revealed that after 8 weeks the cements showed equally and uniformly dense structures with microscopic pores (<1 microm). Both CPCs showed fewer crystal plaques at 8 weeks than at 24 h. This study shows that CPC is not severely changed by its modification for rhTGF-beta1. The prolonged setting time of modified cement may affect the clinical handling but is still within acceptable limits. The compressive strength for both standard and modified cements was within the range of thin trabecular bone; therefore, both CPCs can withstand equal mechanical loading. The faster diminishing compressive strength of modified cement from 24 h to 8 weeks likely results in early breakdown and so might be favorable for bone regeneration. Together with the beneficial effects on bone regeneration from the addition of rhTGF-beta1 to CPC, as shown in our previous studies, we conclude that the envisaged applications for CPC in bone defects are upgraded by the intermixing of rhTGF-beta1. Therefore, the combination of CPC and rhTGF-beta1 forms a promising synthetic bone graft.

Bone Cements↗
PubMed2002

Donor age and mechanosensitivity of human bone cells.

With increasing age the human skeleton decreases in density, thereby compromising its load-bearing capacity. Mechanical loading activates bone formation, but an age-dependent decrease in skeletal mechanoresponsiveness has been described in rats. In this paper we examine whether age-related bone loss is reflected by a decrease in the mechanosensitivity of isolated bone cells from human donors. Bone cell cultures were obtained from 39 donors (males and females) between 7 and 85 years of age. Cultures were challenged with 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) or mechanically stressed by treatment with pulsating fluid flow (PFF; 0.7 +/- 0.03 Pa at 5 Hz for 1 h). The growth capacity of the bone-derived cell population almost halved between 7 and 85 years of age. Basal alkaline phosphatase activity of the cells increased with donor age, while the response to 1,25(OH)2D3, measured as stimulated osteocalcin production, decreased with age. Together this suggests that the cell cultures from older donors represented a more mature, slower-growing cell population than the cultures from young donors. All cell cultures responded to mechanical stress with enhanced release of prostaglandin E2 (PGE2) and I2 (PGI2). The magnitude of the response was positively correlated with donor age, cell cultures from older donors showing a higher response than cultures from younger donors. There was also a positive correlation between time to reach confluency and mechanosensitivity, i.e., the PGE2 response to PFF treatment was higher in bone cell cultures with a slower growth rate. We conclude that bone cell cultures from older donors have a lower proliferative capacity and a higher degree of osteoblastic maturation than younger donors. The higher degree of osteoblastic maturation explains the higher response of the cultures to mechanical stress, in line with earlier studies on chicken bone cells. This study found no evidence for loss of mechanosensitivity with donor age. The reduced growth capacity might, however, be a factor in age-related bone loss.

Adolescent↗
PubMed2002

Transforming growth factor-beta1 incorporation in an alpha-tricalcium phosphate/dicalcium phosphate dihydrate/tetracalcium phosphate monoxide cement: release characteristics and physicochemical properties.

The osteoconductive properties of calcium phosphate cements (CPCs) may be improved by the addition of growth factors, such as recombinant human transforming growth factor-beta1 (rhTGF-beta1). Previously we have shown that rhTGF-beta1 was released from cement enriched with rhTGF-beta1 and subsequently stimulated the differentiation of pre-osteoblastic cells from adult rat long bones. It is unknown whether the addition of rhTGF-beta1 changes the material properties of this alpha-tricalcium-phosphate (alpha-TCP)/tetracalcium-phosphate-monoxide (TeCP)/dicalcium-phosphate-dihydrate (DCPD) cement, and what the characteristics of the release of rhTGF-beta1 from this CPC are. Therefore, in the present study we determined the release of rhTGF-beta1 from cement pellets in vitro. The possible intervening effects of the CPC modification for intermixing rhTGF-beta1 on physicochemical properties were studied by assessing the compressive strength and setting time, as well as crystallinity, calcium to phosphorus ratio, porosity and microscopic structure. Most of the previously incorporated rhTGF-beta1 in the cement pellets was released within the first 48 h. For all concentrations of rhTGF-beta1 intermixed (100 ng-2.5 mg/g CPC), approximately 0.5% of the amount of rhTGF-beta1 incorporated initially was released in the first 2 h, increasing to 1.0% after 48 h. The release of rhTGF-beta1 continued hereafter at a rate of about 0.1% up to 1 week, after which no additional release was found. The initial setting time, nor the final setting time was changed in control cement without rhTGF-beta1 (standard CPC) or in cement modified for rhTGF-beta1 (modified CPC) at 20 degrees C and 37 degrees C. Setting times were more than six times decreased at 37 degrees C compared to 20 degrees C. The compressive strength was initially low for both standard CPC and modified CPC, after which it increased between 24 h and 8 weeks. The compressive strength for the modified CPC was significantly higher compared with standard at 1, 2, and 8 weeks after mixing. X-ray diffraction revealed that both standard and modified CPC changed similarly from the original components into crystalline apatite. The calcium to phosphorus ratio as determined by an electron microprobe did not differ at all time points measured for standard CPC and modified CPC. In both standard CPC and modified CPC the separated particles became connected by crystals, forming a structure in which the particles could hardly be recognised in a densifying matrix with some small pores. The present study shows that the calcium phosphate cement is not severely changed by modification for the addition of rhTGF-beta1. The addition of rhTGF-beta1 in CPC enhances the biologic response as shown in our previous study and did not interfere with the aimed physical and chemical properties as shown in this study. We conclude that the addition of rhTGF-beta1 enlarges the potential of the CPC in bone replacement therapy.

Animals↗
PubMed2002

Effect of recombinant human osteogenic protein-1 on the healing of a freshly closed diaphyseal fracture.

Osteogenic protein-1 (OP-1), or bone morphogenetic protein-7, is an osteoinductive morphogen that is involved in embryonic skeletogenesis and in bone repair. In bone defect models without spontaneous healing, local administration of recombinant human OP-1 (rhOP-1) induces complete healing. To investigate the ability of rhOP-1 to accelerate normal physiologic fracture healing, an experimental study was performed. In 40 adult female goats a closed tibial fracture was made, stabilized with an external fixator, and treated as follows: (1) no injection; (2) injection of 1 mg rhOP-1 dissolved in aqueous buffer; (3) injection of collagen matrix; and (4) injection of 1 mg rhOP-1 bound to collagen matrix. The test substances were injected in the fracture gap under fluoroscopic control. At 2 and 4 weeks, fracture healing was evaluated with radiographs, three-dimensional computed tomography (CT), dual-energy X-ray absorptiometry, biomechanical tests, and histology. At 2 weeks, callus diameter, callus volume, and bone mineral content at the fracture site were significantly increased in both rhOP-1 groups compared with the no-injection group. As signs of accelerated callus maturation, bending and torsional stiffness were higher and bony bridging of the fracture gap was observed more often in the group with rhOP-1 dissolved in aqueous buffer than in uninjected fractures. Treatment with rhOP-1 plus collagen matrix did not result in improved biomechanical properties or bony bridging of the fracture gap at 2 weeks. At 4 weeks there were no differences between groups, except for a larger callus volume in the rhOP-1 plus collagen matrix group compared with the control groups. All fractures showed an advanced stage of healing at 4 weeks. In conclusion, the healing of a closed fracture in a goat model can be accelerated by a single local administration of rhOP-1. The use of a carrier material does not seem to be crucial in this application of rhOP-1.

Absorptiometry, Photon↗
PubMed2002

[The response of bone cells to shear stress].

Loading-induced flow of fluid is a signal for bone cell adaptive responses, but the nature of the flow-derived stimulus which activates the cell is debated. Candidate stimuli include shear stress, streaming potentials and chemotransport. In this study the nature of the cell stimulus was addressed by varying the shear stress, using nitric oxide (NO) and prostaglandin E2 (PGE2) production as a parameter of bone cell activation. Mouse bone cell cultures were treated for 15 minutes with or without pulsating fluid flow (PFF). In a few experiments, dextran was added to the fluid to increase the shear stress without affecting streaming potentials or chemotransport. NO and PGE2 production were dose-dependently stimulated by PFF. Application of dextran in the flow medium enhanced both NO and PGE2 production by bone cells. It was demonstrated that the production of NO and PGE2 by bone cells is enhanced by fluid flow of increasing shear stress. Therefore, the stimulus leading to NO and PGE2 production is shear stress rather than streaming potentials or chemotransport.

Animals↗
PubMed2001

Osteopontin-deficient bone cells are defective in their ability to produce NO in response to pulsatile fluid flow.

Osteopontin (OPN) is a noncollagenous component of bone matrix. It mediates cell attachment and activates signal transduction pathways. In this work, bone cells, cultured from fragments of long bones derived from wild-type and OPN-/- ("knock-out") mice, were exposed to pulsatile fluid flow (PFF) over a 60-min period. The medium was assayed periodically for nitric oxide (NO) and prostaglandin E(2) (PGE(2)) release. OPN+/+ cells exhibited a peak of NO production 5-10 min after the onset of PFF, decreasing to a stable plateau at 15 min; much less NO was produced by the OPN-/- cells. PFF resulted in reduced PGE(2) release by both cell types, although the reduction was less for the OPN-/- cells in the 15-30 min window. Both cell types exhibited a similar enhancement of cyclooxygenase2 mRNA levels 60 min after initiation of PFF. These results suggest that bone cells require OPN to respond fully to PFF as assessed by increased NO and reduced PGE(2) synthesis.

Animals↗
PubMed2001

Different responsiveness of cells from adult and neonatal mouse bone to mechanical and biochemical challenge.

Neonatal rodent calvarial bone cell cultures are often used to study bone cell responsiveness to biochemical and mechanical signals. However, mechanical strains in the skull are low compared to the axial and appendicular skeleton, while neonatal, rapidly growing bone has a more immature cell composition than adult bone. In the present study, we tested the hypothesis that bone cell cultures from neonatal and adult mouse calvariae, as well as adult mouse long bones, respond similarly to treatment with mechanical stress or 1,25-dihydroxyvitamin D3 (1,25(OH)2 D3). Treatment with pulsating fluid shear stress (0.6 +/- 0.3 Pa, 5 Hz) caused a rapid (within 5 min) 2-4-fold increase in NO production in all cases, without significant differences between the three cell preparations. However, basal NO release was significantly higher in neonatal calvarial cells than adult calvarial and long bone cells. The response to 1,25(OH)2 D3), measured as increased alkaline phosphatase activity, was about three times higher in the neonatal cells than the adult cell cultures. We conclude that all three types of primary bone cell cultures responded similarly to fluid shear stress, by rapid production of NO. However, the neonatal cell cultures were different in basal metabolism and vitamin D3 responsiveness, suggesting that cell cultures from adult bone are best used for in vitro studies on bone cell biology.

Alkaline Phosphatase↗
PubMed2001

The production of nitric oxide and prostaglandin E(2) by primary bone cells is shear stress dependent.

Loading-induced flow of interstitial fluid through the lacuno-canalicular network is a likely signal for bone cell adaptive responses. However, the nature of the stimulus that activates the cell is debated. Candidate stimuli include wall shear stress, streaming potentials, and chemotransport. We have addressed the nature of the flow-derived cell stimulus by comparing variations in fluid transport with variations in wall shear stress, using nitric oxide (NO) and prostaglandin E(2) (PGE(2)) production as a parameter of bone cell activation. Adult mouse long bone cell cultures were treated for 15min with or without pulsating fluid flow using the following regimes: Low PFF, mean flow rate 0.20 cm(3)/s, 3 Hz, shear stress 0.4+/-0.12 Pa; Medium PFF, 0.33 cm(3)/s, 5 Hz, 0.6+/-0.27 Pa; and High PFF, 0.63 cm(3)/s, 9Hz, 1.2+/-0.37 Pa. In some Low PFF experiments, 2.8% neutral dextran (mol. wt. 4.98x10(4)) was added to the flow medium to increase the viscosity, thereby increasing the wall shear stress 3-fold to a level similar of the High PFF stimulus, but without affecting streaming potentials or chemotransport. NO and PGE(2) production were stimulated by Low, Medium, and High PFF in a dose-dependent manner. Application of Low PFF using dextran-supplemented medium, enhanced both the NO and PGE(2) response by 3-fold, to a level mimicking the response to High PFF at normal viscosity. These results show that the production of NO and PGE(2) by bone cells can be enhanced in a dose-dependent manner by fluid flow of increasing wall shear stress. Therefore, the stimulus leading to NO and PGE(2) production is the flow-derived shear stress, and not streaming potentials or chemotransport.

Animals↗
PubMed2001

Low-intensity ultrasound stimulates endochondral ossification in vitro.

Animal and clinical studies have shown an acceleration of bone healing by the application of low-intensity ultrasound. The objective of this study was to examine in vitro the influence of low-intensity ultrasound on endochondral ossification of 17-day-old fetal mouse metatarsal rudiments. Forty-six triplets of paired metatarsal rudiments were resected 'en block' and cultured for 7 days with and without low-intensity ultrasound stimulation (30 mw/cm2). At days 1, 3, 5, and 7, the total length of the metatarsal rudiments, as well as the length of the calcified diaphysis were measured. Histology of the tissue was performed to examine its vitality. The increase in length of the calcified diaphysis during 7 days of culture was significantly higher in the ultrasound-treated rudiments compared to the untreated controls (P = 0.006). The growth of the control diaphysis was 180 +/- 30 microm (mean +/- SEM), while the growth of the ultrasound-treated diaphysis was 530 +/- 120 microm. The total length of the metatarsal rudiments was not affected by ultrasound treatment. Histology revealed a healthy condition of both ultrasound-treated and control rudiments. In conclusion, low-intensity ultrasound treatment stimulated endochondral ossification of fetal mouse metatarsal rudiments. This might be due to stimulation of activity and/or differentiation of osteoblasts and hypertrophic chondrocytes. Our results support the hypothesis that low-intensity ultrasound activates ossification via a direct effect on osteoblasts and ossifying cartilage.

Animals↗
PubMed2001

Histology of human alveolar bone regeneration with a porous tricalcium phosphate. A report of two cases.

Porous beta-phase tricalcium phosphate particles (pTCP) (Cerasorb) were used in two patients to restore or augment alveolar bone prior to the placement of dental implants. In one patient, pTCP was used to fill a large alveolar defect in the posterior mandible after the removal of a residual cyst, and in another patient to augment the sinus floor. Biopsies were taken at the time of implant placement, 9.5 and 8 months after grafting, respectively, and processed for hard tissue histology. Goldner-stained histological sections showed considerable replacement of the bone substitute by bone and bone marrow. In the 9.5 months biopsy of the mandible, 34% of the biopsy consisted of mineralised bone tissue and 29% of remaining pTCP, while the biopsy at 8 months after sinus floor augmentation consisted of 20% mineralised bone and 44% remaining pTCP. Bone and osteoid were lying in close contact with the remaining pTCP and were also seen within the micropores of the grafted particles. Tartrate resistant-acid phosphatase (TRAP) multinuclear cells, presumably osteoclasts, were found surrounding, within and in close contact with the pTCP particles, suggesting active resorption of the bone substitute. Remodelling of immature woven bone into mature lamellar bone was also found. No histological signs of inflammation were detected. The limited data presented from these two cases suggest that this graft material, possibly by virtue of its porosity and chemical nature, may be a suitable bone substitute that can biodegrade and be replaced by new mineralising bone tissue.

Absorbable Implants↗
PubMed2001

Transforming growth factor-beta1 incorporated in calcium phosphate cement stimulates osteotransductivity in rat calvarial bone defects.

Bone regeneration of the alveolar crest around dental implants is an important factor in the success of implant use. Calcium phosphate cement can be used as a bone substitute and applied clinically as a paste to fill micro- and macroscopic bone defects. We have shown earlier that the intermixing of the recombinant human transforming growth factor-beta1 (rhTGF-beta1) in hardening calcium phosphate cement stimulated osteoblastic differentiation of rat primary bone cells in vitro. The aim of the present study was to examine whether the similar enrichment with rhTGF-beta1 affects the replacement of calcium phosphate cement by bone (osteotransduction) in calvarial critical size defects (csd) of adult rats. Two bone defects of 5 mm diameter were created bilaterally in each skull of 10 adult male rats. Both defects were filled with 53 mg of calcium phosphate cement without rhTGF-beta1 (control) at one side, and with 10 or 20 ng rhTGF-beta1 at the other side. After 8 weeks, defects with surrounding skull were analysed histologically and histomorphometrically. The addition of rhTGF-beta1 in the cement increased the amount of bone in rat skull defects. This finding coincidences with our in vitro observations, that intermixing of rhTGF-beta1 in calcium phosphate cement stimulates bone cell differentiation. Addition of rhTGF-beta1 stimulated bone formation as indicated by an increased bone volume of 50% and an increased bone/cement contact of 65%, in comparison to control defects with cement without rhTGF-beta1. In addition, rhTGF-beta1 reduced the remaining volume of cement, by 11% at 10 ng rhTGF-beta1, and by 20% at 20 ng rhTGF-beta1 in the cement. Defect closure was not affected. We conclude that the intermixing of rhTGF-beta1 in a fast-setting calcium phosphate cement stimulates bone growth and the osteotransduction of the cement. For bone regeneration procedures around endosseous implants, calcium phosphate cement with rhTGF-beta1 might be an appropriate combination for early osseointegration and implant use.

Animals↗
PubMed2001

Estrogen enhances mechanical stress-induced prostaglandin production by bone cells from elderly women.

Several studies indicate that estrogen may enhance the effects of mechanical loading on bone mineral density in elderly women. This stimulating effect of estrogen could be due to increased sensitivity of bone cells to mechanical stress in the presence of estrogen. The present study was performed to determine whether 17beta-estradiol (E2) enhances mechanical stress-induced prostaglandin production and cyclooxygenase (COX)-2 mRNA expression. We subjected bone cells from seven nonosteoporotic women between 56 and 75 yr of age for 1 h to pulsating fluid flow (PFF) in the presence or absence of 10(-11) M E2 and measured prostaglandin production and COX-1 and COX-2 mRNA expression. One hour of PFF stimulated prostaglandin (PGE2) production threefold, PGI2 production twofold, and COX-2, but not COX-1, mRNA expression 2.9-fold. Addition of E2 further enhanced PFF-stimulated PGE2 production by 1.9-fold but did not significantly affect PGI2 production or COX-2 or COX-1 mRNA expression. E2 by itself did not affect any of the parameters measured. These results suggest that estrogen modulates bone cell mechanosensitivity via the prostaglandin synthetic pathway independently of COX mRNA expression.

Aged↗
PubMed2000

Use of recombinant human osteogenic protein-1 for the repair of subchondral defects in articular cartilage in goats.

The objective of this pilot study was to examine in vivo the potential of recombinant human osteogenic protein-1 (rhOP-1, also called bone morphogenetic protein-7, BMP-7) for treatment of subchondral lesions by induction of new hyaline cartilage formation. Subchondral left knee defects in 17 mature goats were treated with fresh coagulated blood mixed with (1) rhOP-1 combined with collagen (OP-1 device, 400 microgram/mL); (2) rhOP-1 alone (OP-1 peptide, 200 microgram/mL); (3) OP-1 device with small particles of autologous ear perichondrium; (4) OP-1 peptide with small particles of autologous ear perichondrium; or (5) autologous ear perichondrium alone (controls). rhOP-1 was combined with either collagen (OP-1 device) or not (OP-1 peptide). The defects were closed with a periosteal flap. The formation of cartilage tissue was studied by histologic and biochemical evaluation at 1, 2, and 4 months after implantation. One and 2 months after implantation there were no obvious differences between control and rhOP-1-treated defects. Four months after implantation, only one out of three controls (without rhOP-1) showed beginning signs of cartilage formation while all four rhOP-1-treated defects were completely or partly filled with cartilage. A significant linear relationship was found between rhOP-1 concentration and the total amount of aggrecan in the defects. These results suggest that implantation of rhOP-1 promotes cartilage formation in subchondral defects in goats at 4 months after implantation. Therefore, rhOP-1 could be a novel factor for regeneration of cartilage in articular cartilage defects.

Animals↗
PubMed2000

Differential stimulation of prostaglandin G/H synthase-2 in osteocytes and other osteogenic cells by pulsating fluid flow.

Mechanical stress produces flow of fluid in the osteocytic lacunar-canalicular network, which is likely the physiological signal for the adaptive response of bone. We compared the induction of prostaglandin G/H synthase-2 (PGHS-2) by pulsating fluid flow (PFF) and serum in osteocytes, osteoblasts, and periosteal fibroblasts, isolated from 18-day-old fetal chicken calvariae. A serum-deprived mixed population of primarily osteocytes and osteoblasts responded to serum with a two- to threefold induction of PGHS-2 mRNA. Serum stimulated PGHS-2-derived PGE(2) release from osteoblasts and osteocytes but not from periosteal fibroblasts as NS-398, a PGHS-2 blocker, inhibited PGE(2) release from osteocytes and osteoblasts with 65%, but not that from periosteal fibroblasts. On the other hand PFF (0.7 Pa, 5 Hz) stimulated (3 fold) PGHS-2 mRNA only in OCY. The related PGE(2) response could be completely inhibited by NS-398. We conclude that osteocytes have a higher intrinsic sensitivity for loading-derived fluid flow than osteoblasts or periosteal fibroblasts.

Animals↗
PubMed2000

Transforming growth factor-beta1 incorporated during setting in calcium phosphate cement stimulates bone cell differentiation in vitro.

Growth stimulation of periimplant tissues by growth factors like transforming growth factor-beta1 (TGF-beta1) may increase the indication for and success of implant use. Calcium phosphate as a material for implants or for coating of implants is known for its good biologic interaction with bone. Therefore, calcium phosphate implants combined with TGF-beta1 might improve osseointegration. In this study we hypothesise that the addition of recombinant human TGF-beta1 (rhTGF-beta1) to calcium phosphate cement (CPC) affects the differentiation of bone cells growing on the cement layer. rhTGF-beta1 incorporated during setting in a CPC layer at 20 ng rhTGF-beta1/60 mg cement was found to be gradually released into tissue culturing medium leading to a 20% release after 24 h. Two cell populations were obtained from collagenase-treated fragments of adult rat long bones: preosteoblastic cells, which were released by the collagenase treatment, and osteoblastic cells, which grew from the collagenase-stripped bone fragments. Both cell populations were tested for their osteoblastic characteristic phenotype by measuring their alkaline phosphatase (ALP) activity after vitamin D treatment and cyclic AMP after parathyroid hormone stimulation. After preculture the cells were plated on a layer of CPC containing 0 (control), 10, or 20 ng rhTGF-beta1/60 mg CPC. Bone cell differentiation was analyzed after 10 days by measuring the ALP activity, as well as the protein content of the cell layer. Incorporation of rhTGF-beta1 in the CPC did not change the ALP activity in osteoblastic cells, but a significant (analyzed by multivariate analysis of variance) increase was observed in preosteoblastic cells. Incorporation of 10 ng of rhTGF-beta1 in 60 mg of CPC increased the ALP activity in preosteoblastic cells by threefold and 20 ng rhTGF-beta1/60 mg CPC increased it by fivefold. The total protein content was not affected by rhTGF-beta1 in either of the cell populations. We conclude that rhTGF-beta1 incorporated during setting in CPC stimulates the differentiation of preosteoblastic cells in vitro. These results provide a basis for further studies on the use of this combination as an implant material in vivo.

1-Methyl-3-isobutylxanthine↗